Thromboxane and Prostacyclin in Platelet/Blood Vessel Interaction: A Commentary

  • J. M. Ritter
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 84)

Abstract

Myocardial infarction is usually caused by thrombosis in a coronary artery occurring on a ruptured atheromatous plaque, and similar pathology underlies crescendo angina and sudden ischaemic death (1). Platelets are the main cell type present in such arterial thrombi. It is also possible that platelets contribute to the development of atheroma (2,3) though this is unproven. Cyclo-oxygenase products (prostanoids) are one among several families of endogenous biologically active substances synthesised by activated platelets and damaged blood vessels which probably influence thrombosis. Whether prostanoids also influence atheroma formation is uncertain. The main cyclo-oxygenase product of platelets is the pro-aggregatory vasoconstrictor thromboxane (TX) A2, while that of arteries is the anti-aggregatory vasodilator prostacyclin (PGI2). Other substances produced by platelets and blood vessels which may function as mediators include platelet activating factor, nucleotides, amines and peptides. These may be at least as important as prostanoids in thrombosis. However, current interest in prostanoids is justified by clinical trials which have demonstrated that the cyclo-oxygenase inhibitor aspirin is partially effective in some vaso-occlusive disorders (4–7).

Keywords

Foam Lipase Aspirin Prostaglandin Charcoal 

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Copyright information

© Martinus Nijhoff Publishing, Boston 1988

Authors and Affiliations

  • J. M. Ritter
    • 1
  1. 1.Department of Clinical PharmacologyRoyal Postgraduate Medical SchoolLondonUK

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